Type 5 diabetes: a 70-year perspective and its implications for the Americas

Summary

Type 5 Diabetes (T5DM) was first identified by Hugh-Jones in Jamaica in 1955 as J-type diabetes. Since then, multiple reports from various countries have supported the idea that T5DM differs from other known forms of diabetes. Common features that distinguish T5DM include a body mass index of <18.5 kg/m², low hepatic fat mass, low C-peptide concentrations, normal insulin sensitivity, and absence of ketoacidosis. Despite this unique phenotype, T5DM is often missed or misdiagnosed, potentially resulting in underreporting, though the magnitude is unknown. While the majority of Latin America and the Caribbean are experiencing a nutritional transition, chronic undernutrition still exists in some regions facing food insecurity and geopolitical conflicts, thus raising the risk for incident T5DM. This paper aims to highlight the 70-year history of T5DM, which began in the Americas, and proposes refocusing our attention on this underexplored but critical condition, which will probably continue to affect many individuals in the Americas.

Introduction

The International Diabetes Federation (IDF) officially recognized type 5 diabetes (T5DM) in April 2025, following reports from several regions indicating that this condition warrants a distinct classification. T5DM is commonly seen in young (age <30 years), lean (BMI <18.5 kg/m²) individuals from low- and middle-income countries (LMICs).¹ Other commonly reported features include low C-peptide levels (higher than in type 1 diabetes (T1DM) and lower levels than in type 2 diabetes (T2DM)), no history of ketoacidosis, and no evidence of insulin resistance.¹ The classification of T5DM has been proposed to address a critical gap in the current diabetes classification, as it is distinct from the forms of diabetes currently referred to as types 1, 2, 3, and 4. In addition to the commonly known types 1 and 2 diabetes, Type 3c diabetes is recognized by the American Diabetes Association as diabetes mellitus secondary to chronic pancreatitis and pancreatic cancer.² Other studies have proposed the term “type 3 diabetes” for Alzheimer's disease, describing it as a brain-specific form of diabetes with molecular features overlapping types 1 and 2.3, 4, 5, 6 Additionally, a non-autoimmune form of diabetes occurring in elderly lean individuals with hepatic insulin resistance has been termed “type 4 diabetes”.⁷ Since the designations “type 3” and “type 4” diabetes are already used in literature indexed in relevant databases, the IDF and an international consensus group proposed that this form of diabetes be classified as “type 5 diabetes”.¹ This classification aims to reduce confusion arising from the prior use of multiple overlapping terms for this condition⁸ and to improve diagnosis and management, as its misclassification can lead to inappropriate treatment and serious adverse outcomes.¹

Although T5DM was first reported as ‘J-type diabetes’ in Jamaica 70 years ago, there is a dearth of research on this disease in the Americas region, and most subsequent research has been focused on South Asia and Sub-Saharan Africa. Since significant pockets of undernutrition exist in the Americas, especially in Central and South America, individuals in these areas are at high risk for T5DM. As a result, more research is required to determine the prevalence of T5DM in the Americas and to develop specific diagnostic criteria and management guidelines appropriate for this region. This article aims to revisit the history of T5DM since its first description in 1955, analyze its implications for the Americas, and promote regional discussions on the diagnosis, management, and prevention of this underrecognized form of diabetes.

Search strategy and selection criteria

PubMed database was searched for articles describing the T5DM phenotype, covering the period from 1955 to 2025. The following MeSH terms were used in various combinations: Diabetes Mellitus, Pancreatic; Malnutrition; Undernutrition; Protein-Energy Malnutrition; Thinness; Body Mass Index; Insulin Secretion; Ketosis. Additional text words “ketosis-resistant” and “BMI” were used to capture relevant articles not indexed under MeSH.

History (1955–1999)

In 1955, Phillip Hugh-Jones from the University of the West Indies (UWI) published his observations of 215 Jamaicans with diabetes who were studied over an 18-month period.⁹ He used the terminology “type 1 diabetes” and “type 2 diabetes” for the first time in his publication on diabetes in Jamaica. In his classification, he used the descriptor “type 1” to describe 12% of the sample who were thin, ketosis-prone and insulin dependent, and “type 2” for the 80% who had obesity (“lipoplethoric”) and diabetes.⁹ However, 13 (6%) children and adults under the age of 40 years who were young, thin, with little or no ketosis, and needed large doses of insulin (generally >80 units/day) to control glucosuria and to maintain their weight were called “Type-J” (J represented Jamaica).⁹ Higher requirements for insulin led the researchers to note that J-type diabetes may be associated with insulin resistance, which may have been due to uncorrected hyperglycemia at the time of study.⁹ These individuals did not show evidence of ketosis even if the insulin was withdrawn. Additionally, they had a lower weight-to-height ratio compared to the mean values and consumed less protein than those with T1DM and T2DM.⁹

Hugh-Jones did not find a dietary cause, although he considered the possibility that consumption of bush teas may interfere with carbohydrate metabolism, which could lead to diabetes. Three individuals underwent liver biopsies, which revealed no histological abnormalities and normal glycogen content, similar to T1DM, rather than the changes in hepatic fat content typically seen in T2DM.⁹ He concluded, “Whether type-J cases represent a clinical entity wholly different from type-1 cases, or are merely this variety of diabetes behaving unusually, needs further study. In their age and mode of onset and their liver biopsy, they resemble type-1 cases, but their insulin resistance and relative lack of ketosis suggest a supply of free insulin”.⁹

Even in the subsequent early years, there was some controversy about the existence of this unique form of diabetes. In 1961, Tulloch and Macintosh followed up on the patients included in the observations by Hugh-Jones and expanded the sample.¹⁰ They concluded that type-J was a subtype of patients with poorly controlled T2DM, and they changed the nomenclature subtly to “J-type.” It was later named “phasic insulin-dependent diabetes” since longer-term studies seemed to show intermittent periods of insulin requirement.¹¹ Since those descriptions, it has been reported in many countries of Sub-Saharan Africa and South Asia. Extensive studies in India confirmed the lack of ketosis and the high insulin requirement.¹² The studies strongly demonstrated the coexistence of protein-energy malnutrition in these patients, suggesting it as a possible etiological factor^12,13 and proposed a scoring system to make the diagnosis. Like Hugh-Jones, they also considered that undetermined environmental (food) toxins could play a role.¹⁴

As a result, in 1985, the World Health Organization (WHO) Expert Committee on Diabetes included Malnutrition-Related Diabetes Mellitus (MRDM) as a separate form of diabetes mellitus, with protein-deficient pancreatic diabetes (PDPD) as its subtype.¹⁵ Subsequently, Morrison and Ragoorbirsingh in Jamaica also showed increased echogenicity of the pancreas compared to patients with T1DM and T2DM, thus suggesting exocrine or parenchymal disease, similar to that seen in severe undernutrition, i.e., the cadavers of infants with severe acute malnutrition (SAM) and canine models.^11,16 Plant toxins, such as those found in cassava and bush teas, commonly used in the region, were not definitively found to play a pathogenic role.¹⁷ Insulin binding to its receptors was reduced in erythrocytes and leukocytes compared to patients with T1DM and T2DM, which was attributed to decreased availability of receptor sites.¹¹ Notably, their subjects also had severe hyperglycemia (HbA1c 16.1 ± 1.2%) and significantly more microalbuminuria.¹¹

Although J-type diabetes was postulated to be associated with undernutrition, the pathophysiological mechanisms were not clearly understood. The forms of undernutrition that increased the risk of MRDM were also unclear. Additionally, whether a deficiency in only macronutrients (i.e., protein and calories) or micronutrients (such as zinc) or a combination of both led to a higher risk of MRDM was poorly understood. As a result, in 1999, the WHO removed the class of MRDM from the diabetes classification, stating that “Whilst it appears that malnutrition may influence the expression of several types of diabetes, the evidence that diabetes can be caused by malnutrition or protein deficiency per se is not convincing”.¹⁸

Role of undernutrition in early life and adulthood (2000–2020)

Despite the removal of its classification by the WHO, several reports of MRDM have been published globally, including in Jamaica, where this type of diabetes was first reported, supporting the hypothesis of its association with undernutrition, particularly from early life to later life.⁸ Concurrent with Hugh-Jones’ description of the type-J diabetes, the University of the West Indies established the Tropical Metabolism Research Unit (TMRU) to investigate and develop treatment protocols for infants with SAM, given that protein-energy malnutrition was a significant public health issue in the region.¹⁹ Infants with SAM had two distinct phenotypes—severe wasting without nutritional edema (i.e., marasmus), and moderate wasting with nutritional edema and high mortality (i.e., kwashiorkor). There may also be developmental differences, as children with marasmus were often born with low birth weights, about 333 g less than those with kwashiorkor.²⁰ Clinical studies conducted in the 1990s and 2000s revealed physiological differences between the phenotypes. In response to the acute phase of SAM, children with marasmus were more able to perform vigorous gluconeogenesis, lipolysis, and proteolysis to provide glucose and free fatty acids for sustaining energy metabolism.^21,22 Although they were glucose intolerant to a similar degree, some studies suggest that this is primarily due to impaired insulin secretion^23,24 rather than insulin resistance. In general, the changes in glucose metabolism resolve after nutritional rehabilitation.^23,25,26

Investigators in Jamaica pioneered research on the long-term effects of severe undernutrition, following a cohort of adult survivors up to 50 years post-hospitalization. In an assessment of glucose metabolism using oral glucose tolerance tests, fasting glucose levels were similar in marasmus survivors, kwashiorkor survivors, age-, sex-, and BMI-matched community controls (CCs), and age- and birth weight-matched controls (BWs).²⁷ However, marasmus survivors had significantly higher rates of glucose intolerance (odds ratio 10.9; 95% confidence interval (CI) 2.1–55) compared to kwashiorkor survivors, CC, and BWs. Insulin sensitivity was similar in marasmus and kwashiorkor survivors and both control groups; however, marasmus survivors exhibited markedly reduced insulin secretion and oral disposition indices compared to kwashiorkor survivors and both control groups.²⁷ The degree of wasting during infancy correlated with the 2-h glucose levels in adults. Birth weight correlated with the fasting glucose levels.²⁷

Furthermore, in a subset of adult marasmus and kwashiorkor survivors and matched community participants who underwent hyperinsulinemic-euglycemic clamps, insulin sensitivity and clearance were similar across all three groups. Neither wasting nor stunting in infancy was linked to adult insulin sensitivity or clearance.²⁸ Notably, within this adult cohort of undernutrition survivors, those diagnosed with marasmus as children remained thinner and shorter as adults compared to those diagnosed with kwashiorkor.²⁹ An epigenome-wide association study revealed 63 differentially methylated genes in the muscles of marasmus survivors, with critical gene nodes involved in growth, glucose metabolism (including pancreatic function), and immunity.³⁰

While early-life nutritional deficits can program long-term metabolic dysfunction, resulting in an elevated risk of adult diabetes, these findings suggest that childhood marasmus is specifically linked to worse pancreatic β-cell function in adulthood, leading to a higher risk of glucose intolerance, even with optimal insulin sensitivity. These studies align with a broader body of evidence linking childhood undernutrition to adult metabolic disease, but add nuance by distinguishing between marasmus and kwashiorkor, demonstrating that survivors of marasmus exhibit pancreatic β-cell deficits. In this Afro-Caribbean cohort of adult SAM survivors, those with marasmus who had lower birth weight were more wasted and stunted at the time of hospitalization and remained thinner and shorter as adults compared to those who had kwashiorkor, which may represent one model for T5DM. Indeed, these adult marasmus survivors, with reduced pancreatic β-cell function and little to no insulin resistance, are similar to cases of T5DM previously reported in Jamaica as well as in India and Africa. The studies confirm that the persistent metabolic issue is primarily related to pancreatic-β cells, rather than insulin resistance or clearance, and suggest the importance of early nutritional interventions to preserve pancreatic-β cell capacity and to reduce the risk of later diabetes vulnerability.

Other data on adult survivors are few, but in general, the experience of famine in infancy and childhood can increase the risk of diabetes in later life. Epidemiological studies show adult survivors of famine (such as in the Netherlands, China, Nigeria) have more glucose intolerance than those not exposed, especially if the starvation occurred in childhood.31, 32, 33 In a meta-analysis, early-life famine exposure was associated with a 1.36-fold increased relative risk (95% CI 1.12–1.65) for those exposed during fetal-infant life, but no association was observed for childhood exposure.³⁴ Young Mexican men who had SAM in infancy were more glucose intolerant and hyperinsulinemic compared to controls.³⁵ However, they were not less insulin sensitive than controls, except when matched for high levels of intra-abdominal fat.³⁶ Notably, they did not report any measure of pancreatic β-cell function, nor did they differentiate the participants by nutritional edema.

Recent metabolic studies and the classification of type 5 diabetes

The most definitive description of metabolic characteristics of T5DM thus far comes from a study by Lontchi-Yimagou et al., in which the metabolic characteristics of individuals with low BMI and diabetes (now called “type 5 diabetes”) were compared with subjects with T1DM, T2DM, overweight individuals without diabetes, and controls with low BMI.³⁷ Lean individuals with diabetes were selected based on the WHO definition of MRDM from 1985. While choosing these subjects, the researchers carefully excluded individuals with a significant history of alcoholism, documented history of ketoacidosis, presence of autoantibodies, chronic kidney disease, coexistent infection, liver dysfunction, any known maturity-onset diabetes of the young (MODY) genes, any genes for lipodystrophy, radiological features of atrophy or calcifications in the pancreas, family history suggestive of young-onset diabetes, and those from higher socioeconomic status.³⁷ The study reported that lean subjects with diabetes were stunted in linear growth, consistent with findings of early-life undernutrition. Furthermore, they had significantly lower truncal and total fat mass than subjects with T2DM and overweight subjects without diabetes.³⁷ The investigators conducted complex hyperinsulinemic-euglycemic clamp studies to measure hepatic and peripheral insulin sensitivity. Insulin secretion levels were measured using C-peptide deconvolution techniques, following correction of glucotoxicity.

The research demonstrated that lean subjects with diabetes had more severe insulin secretion defects and normal insulin sensitivity compared to the lean group without diabetes and those with T2DM.³⁷ The lean subjects with diabetes also showed significantly lower endogenous glucose production compared to those with T2DM. In contrast, glucose uptake was notably higher in the lean subjects with diabetes relative to the T2DM group.³⁷ Also, these individuals did not have a history of diabetes ketoacidosis, which is more common in T1DM. Thus, a marked defect in insulin secretion, normal insulin sensitivity, very low hepatic fat mass, and absence of ketoacidosis differentiate T5DM from other existing diabetes phenotypes (Table 1)^8,38, 39, 40 and warrant classification as a separate category of diabetes. In addition to this study, several other publications have also supported the notion that T5DM represents a distinct phenotype of diabetes.^8,41,42

Table 1.

Reported characteristics of types 1, 2, and 5 diabetes.

Characteristic	Type 5	Type 1	Type 2
BMI (kg/m2)a	<18.5	Traditionally normal (18.5–24.9), but increasingly associated with overweight/obesity	Traditionally overweight/obese, now recognized to occur in some populations at BMI 20–25
Age of onseta	<30 years	Mostly <18 years	Traditionally third decade and beyond, now includes adolescence in western countries
History of childhood malnutrition	Strong	–	Possible, particularly in low resource settings
Hyperglycemia at diagnosisb	Severe	Variable	Variable
Ketosis	Absent	Present	Absent
Hepatic fat content	Very low	Low	Moderate–High
Pancreatic-β cell function	Impaired	Impaired	Somewhat preserved, further impairment with progression of disease
Insulin sensitivity	Normal	Can be somewhat impaired	Impaired

This table was adapted from the article “Atypical forms of diabetes mellitus in Africans and other non-European ethnic populations in low- and middle-income countries: a systematic literature review” by Bavuma et al.⁸ and additional data incorporated from references.^9,37 This work is licensed under a Creative Commons Attribution 4.0 International License. BMI, body mass index; MODY, maturity-onset diabetes of the young; TD1, type 1 diabetes; TD2, type 2 diabetes.

^aFor type 2 diabetes, there may be heterogeneity across age groups and BMI in some populations.

^bHyperglycemia at diagnosis of types 1 and 2 is variable, depending on frequency of screening and rate of onset.

It is critical to note that the phenotype of T5DM includes remarkably low hepatic fat in very lean (BMI ∼ 18.5 kg/m²), insulin sensitive individuals with non-ketosis-prone diabetes; Lontchi-Yimagou et al. reported hepatic fat levels of 0.38% and 0.34% (geometric means) in the lean diabetes and lean control groups, respectively.³⁷ Indeed, these very low liver fat levels parallel the original findings by Hugh Jones in Jamaica, as described above. To put these measurements in context, while hepatic fat levels of less than 5.5% have been proposed to be “normal” in North America, a recent study reported that considerably lower hepatic fat levels (>1.85%) in individuals with a BMI ∼22 kg/m² are associated with lower insulin sensitivity, particularly in individuals of Asian-Indian background.⁴³ Indeed, this US-based study found hepatic fat levels of 0.76% and 0.48% (both geometric mean) in lean individuals of Asian Indian and non-Asian Indian backgrounds, respectively. These findings emphasize the considerable impact of both BMI and ethnicity on hepatic fat, important factors to consider when approaching patients with very low BMI in the Americas. Additionally, given the strong association between liver fat and insulin sensitivity, it is crucial to compare hepatic fat in people with and without diabetes at similar BMI levels, and to reconsider the “normal” hepatic fat cut-off values as we work to better characterize T5DM.

In January 2025, researchers from the United States, Jamaica, the United Kingdom, Germany, Sweden, Denmark, India, Bangladesh, Sri Lanka, Côte D'Ivoire, Ethiopia, Uganda, and Rwanda convened at an International Consensus Meeting in India to discuss the classification, pathophysiology, and management of diabetes in individuals who are lean and experiencing undernutrition.¹ Endocrinologists, diabetes researchers, including epidemiologists and basic scientists with scientific expertise and decades of experience in providing clinical care to patients with diabetes from around the world, were invited to the consensus meeting.¹ Additionally, leaders from the National Institutes of Health, the American Diabetes Association, and the IDF also participated in the meeting.¹ The meeting featured presentations and discussions on the clinical and study findings from the invited diabetes experts. The meeting participants overwhelmingly agreed that this form of diabetes deserved a distinct classification and were in favor of naming it Type 5 Diabetes.¹ Following this crucial consensus meeting, on April 7, 2025, the International Diabetes Federation officially inaugurated the IDF Type 5 Diabetes Working Group at the IDF World Diabetes Congress in Bangkok, Thailand. The working group is tasked with a 2-year mandate to facilitate global collaborations to advance more research and develop diagnostic and management guidelines for T5DM. The working group, comprising a core coordinating committee and several subcommittees, will meet regularly over the next two years to complete this mandate.

The Americas: from history to the future/implications for the future

Type 5 diabetes, previously described as MRDM, was first reported in Jamaica but has received limited attention in the subsequent 7 decades, resulting in few studies from the Americas. Nonetheless, available evidence suggests that the condition remains present in parts of Central and South America, as well as among socioeconomically marginalized populations in North America. As per the 2022 estimates of the Food and Agriculture Organization (FAO), the prevalence of severe food insecurity is 13% in Latin America and the Caribbean, compared to 11.3% in the world (as per FAO, severe food insecurity refers to situations when individuals likely lack enough food, experience hunger, and at the most extreme, have to go without eating.) The countries with high prevalence of severe food insecurity in this region include Haiti (42.9%), Jamaica (25.6%), Honduras (23.5%), Dominican Republic (22%), and Guatemala (21.1%).⁴⁴ The data also shows that, although the prevalence of hunger decreased from 7% in 2021 to 6.5% in 2022 in Latin America and the Caribbean, the prevalence remained 0.9 percentage points above the level registered in 2019, that is, before the Covid-19 pandemic.⁴⁴ The impact of Covid-19 on undernutrition cannot be ignored, as the pandemic was associated with an increased rate of hunger and undernourishment in Latin American and Caribbean countries.⁴⁴ Given the potential impact of the pandemic on food access in this region, undernourishment data is presented between the years 2017 and 2024 (Table 2), although the likely impact on reporting during this period is not known. Additionally, although hunger in Latin America and the Caribbean is categorized as low, ≤9.9 on a 100 point scale of Global Hunger Index (a tool comprised of indicators of undernourishment, child stunting, child wasting, and child mortality, used to comprehensively measure and track hunger at regional, national and global levels), this is the only region where hunger has worsened since 2016.⁴⁴ This is due to rising food inflation, fertilizer prices, national debt, crime rates, and the impact of severe weather from climate change, which magnify health inequalities and extreme poverty.⁴⁵

Table 2.

Latin American and Caribbean countries with an undernourishment rate > 5% from 2017 to 2024.

Country	2017–2019	2020–2022	2022–2024
	Prevalence of undernourishment	Prevalence of undernourishment	Prevalence of undernourishment
Haiti	41.2	47.8	54.2
Bolivia	13.7	19.1	21.8
Honduras	13.1	14.1	14.8
Venezuela	23.4	13.0	5.9
Nicaragua	15.5	17.0	17.1 (2021–2023)
Ecuador	11.3	13.6	12.1
Guatemala	14.0	12.9	11.8
Trinidad and Tobago	7.2	11.7	11.2
Suriname	9.0	9.3	9.7
Jamaica	6.3	7.6	7.7
El Salvador	6.8	7.0	6.7
Peru	6.0	6.5	6.9
Dominica	5.5	5.1	3.6
Colombia	4.2	4.1	3.9
Dominican Republic	5.6	5.5	3.6
Panama	5.0	5.3	5.7
Belize	5.3	5.1	7.0
St. Vincent and Grenadine	5.1	5.8	6.1
Paraguay	2.7	3.9	5.2

Countries in this region with a recorded undernourishment rate >5% at any point from 2017 to 2024 were included. For comparison, the undernutrition rate in Canada and the United States is <2.5% and in Mexico it is 2.7%, so these North American countries were not included. Of note, the percent undernourishment in Nicaragua is from 2021 to 2023 due to a lack of available data from 2022 to 2024. All of the numbers from the table were sourced from https://www.fao.org/faostat/en/#data/FS. However, given various geopolitical situations in the region, there may be errors in reporting, which may warrant some caution in interpreting the data. Adapted from Food and Agriculture Organization of the United Nations (2025). FAOSTAT Statistical Database. Available from: https://www.fao.org/faostat/en/#data/FS. Accessed 10 October 2025.

The prevalence of undernourishment is higher than 5% in at least 15 countries in the Latin America and Caribbean region (Table 2 and Fig. 1). FAO defines undernourishment as a condition where an individual does not get enough food on average to meet the dietary energy needed for a normal, active, and healthy life. It is essential to note that, although the prevalence of undernourishment in Brazil was 3.2% from 2021 to 2023, the number of people affected was 6.7 million.⁴⁴ It is postulated that this issue is more prevalent in the northern and northeastern regions of the country, where food insecurity is also higher, particularly in children.⁴⁶ Further, an estimated 33 million people in Brazil experience hunger, reflecting a substantial burden, and raising concern regarding the presence of undiagnosed T5DM, especially in those who are thin and receive a new diagnosis of T1DM.⁴⁷

Fig. 1.

Latin American and Caribbean Countries with Undernourishment Rates > 5% from 2022 to 2024. Data obtained from Food and Agriculture Organization of the United Nations (2025). FAOSTAT Statistical Database. Accessed 10 October 2025. Created in BioRender. Shamamian, M. (2025) https://biorender.com/oj6asi8.

Individuals who are exposed to severe hunger and chronic undernutrition or reside in areas of conflict, such as Haiti,⁴⁵ are at greater risk of developing T5DM.^1,48,49 Food insecurity, inequitable access to healthcare, and restricted availability of insulin may further contribute to adverse outcomes. Although several reports have been published on the burden of diabetes in Latin America and the Caribbean,50, 51, 52, 53 the specific data on people with low BMI and diabetes are minimal.54, 55, 56, 57 A cross-sectional study using nationally representative data on BMI and diabetes risk in 57 LMICs shows that the risk of diabetes at BMI <18.5 kg/m² is highest in men and second highest in women from Latin America and the Caribbean, compared to the risk at lower BMI in other regions.⁵⁵ Another study examining diabetes prevalence across the BMI spectrum in rural indigenous Guatemala found that among subjects with BMI <18.5 kg/m², 14.29% had diabetes.⁵⁷ Research also shows that racial and ethnic minorities have a higher burden of diabetes at lower BMI levels, even in high-income countries such as the United States. Data from the Patient Outcomes Research To Advance Learning (PORTAL) Network, which includes 10 sites across three integrated healthcare systems in the United States show that the prevalence of diabetes in individuals with BMI <18.5 kg/m² in Black (9.9%), Hispanic (8.8%), Asian (7.3%), Hawaiian/Pacific Islander (10.2%), and American Indian/Alaskan Native (7.2%) was higher than White (3.5%) study participants, with an overall prevalence in this BMI category was 5.2%.⁵⁴

Although there is extensive literature on diabetes prevalence in the Americas, specific data on T5DM are limited. The insufficient data may be due to the exclusion of individuals with a BMI <18.5 kg/m² from many studies on diabetes. In some studies, primarily describing T2DM, low BMI individuals were included, but data for people with BMI <18.5 kg/m² were not separately analyzed.^53,55,58 Since what is now referred to as T5DM was previously known by several different names, this may have led to underdiagnosis of this condition. The diagnostic criteria currently under development should help to specifically identify undiagnosed cases of T5DM, which may add substantially to the recognized number of cases in this region.^39,53 Given that T5DM is a very recent classification and WHO's classification of MRDM was removed in 1999, it is likely that reports of diabetes in the intervening years were not likely to focus on the category of patients with BMI <18.5 kg/m². Thus, available data reporting the prevalence of “types 1 and 2” diabetes may need to be reanalyzed to find misdiagnosed and missed cases of T5DM. Further research in Central and South America is necessary to enhance awareness of the condition among healthcare providers. Once the diagnostic criteria are established by the IDF Type 5 Diabetes Working Group, these criteria will need to be validated for their applicability in the Latin American and Caribbean regions. Expanding regional diabetes registries would help to appreciate the disease burden and study patients with T5DM to monitor their response to treatment and prognosis.

Public health implications

Many regions in Latin America and the Caribbean have been undergoing nutritional transitions, in the setting of improving gross domestic products (GDP) over the past three decades, which has led to the coexistence of T2DM and T5DM phenotypes.^53,56,58,59 As noted above, given limited awareness of T5DM and the high prevalence of T1DM and T2DM, individuals with T5DM may often be misdiagnosed as one of the commonly occurring forms of diabetes and thus managed inappropriately. If they are diagnosed with T1DM and are given higher amounts of insulin, it may lead to a dangerous risk of hypoglycemia in patients with T5DM, particularly if they have a lower calorie intake. On the other hand, if they are diagnosed with T2DM and are advised to restrict their calorie intake or are prescribed medicines such as GLP-1 receptor agonists, the resulting weight loss would be detrimental. Therefore, creating awareness among healthcare providers on this type of diabetes is extremely important to identify and appropriately manage cases with T5DM. This would also encourage data collection on early life nutrition and/or anthropometry to identify individuals at high risk of developing T5DM and provide nutritional rehabilitation to prevent its development. More data are also needed to define optimal rates of growth that balance the risks of T5DM versus early onset of T2DM. Prevention of T5DM would also reinforce another indication of the need to implement Sustainable Development Goal 2, which aims to achieve zero hunger by 2030.

Conclusions

The entity now classified as T5DM has been reported in many countries over the past 70 years, mostly from low-resource settings. Although it has been less frequently reported in the Americas, it is likely to be present but underdiagnosed in areas of chronic hunger and undernutrition. In some cases, patients with this form of diabetes are misdiagnosed with T1DM and T2DM and mismanaged, leading to severe complications. The gaps in identifying and managing T5DM highlight the need for more research to establish clear diagnostic criteria and effective treatment strategies for affected individuals. This is especially critical in regions with food insecurity and undernutrition, including Latin American and Caribbean countries, where individuals may be at higher risk. There is also a need to identify unrecognized or missed cases in this region using a multifaceted approach. Improving and expanding health surveillance systems in high-risk populations should be a top priority, with efforts centered on identifying risk factors and new cases through patient screening. Healthcare providers should be informed about appropriate diagnostic and management strategies through updating higher education curricula in the health field. Medical literature and media should also share updated findings to ensure that accurate and timely information reaches both patients and healthcare professionals, thereby fostering improved awareness of this issue. Given what is known about the risk of T5DM in this region, particularly in areas with high rates of undernutrition, it is vital to continue efforts to improve the identification and management of affected individuals.

Contributors

Pradnyashree Wadivkar (PW): writing: original draft, writing—review and editing, investigation, project administration.

Debbie S Thompson (DST): writing: original draft, writing—review and editing, investigation.

Meredith Shamamian (MS): writing—review and editing, creation of figure.

Meredith Hawkins (MH): Conceptualization, writing—review and editing, supervision.

Michael S Boyne (MSB): Conceptualization, writing: original draft, writing—review and editing, investigation, supervision.

Editor note

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Declaration of interests

We declare no conflict of interest.